MyD88 and TRIF mediate the cyclic adenosine monophosphate (cAMP) induced corticotropin releasing hormone (CRH) expressio
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MyD88 and TRIF mediate the cyclic adenosine monophosphate (cAMP) induced corticotropin releasing hormone (CRH) expression in JEG3 choriocarcinoma cell line Andy Uh1, Charles F Simmons1, Catherine Bresee2, Nasif Khoury1, Adrian F Gombart3, Richard C Nicholson4, Hande Kocak5 and Ozlem Equils*1 Address: 1Ahmanson Department of Pediatrics, Room 4221, Steven Spielberg Pediatric Research Center, Burns and Allen Research Institute, Cedars-Sinai Medical Center, David Geffen School of Medicine at UCLA, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA, 2Samuel Oschin Comprehensive Cancer Institute Biostatistics Core, Cedars-Sinai Medical Center, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA, 3Linus Pauling Institute; Department of Biochemistry and Biophysics; ALS 2011, Oregon State University; Corvallis, OR 97331-7305, USA, 4Mothers and Babies Research Center, Hunter Medical Research Institute, John Hunter Hospital, Newcastle, Australia and 5Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA Email: Andy Uh - [email protected]; Charles F Simmons - [email protected]; Catherine Bresee - [email protected]; Nasif Khoury - [email protected]; Adrian F Gombart - [email protected]; Richard C Nicholson - [email protected]; Hande Kocak - [email protected]; Ozlem Equils* - [email protected] * Corresponding author
Published: 17 July 2009 Reproductive Biology and Endocrinology 2009, 7:74
doi:10.1186/1477-7827-7-74
Received: 6 January 2009 Accepted: 17 July 2009
This article is available from: http://www.rbej.com/content/7/1/74 © 2009 Uh et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Classically protein kinase A (PKA) and transcription factor activator protein 1 (AP-1) mediate the cyclic AMP (cAMP) induced-corticotrophin releasing hormone (CRH) expression in the placenta. However enteric Gram (-) bacterial cell wall component lipopolysaccharide (LPS) may also induce-CRH expression via Toll like receptor (TLR)4 and its adaptor molecule Myd88. Here we investigated the role of MyD88, TRIF and IRAK2 on cAMP-induced CRH promoter activation in JEG3 cells in the absence of LPS/TLR4 stimulation. Methods: JEG3 cells were transfected with CRH-luciferase and Beta-galactosidase expression vectors and either empty or dominant-negative (DN)-MyD88, DN-TRIF or DN-IRAK2 vectors using Fugene6 (Roche). cAMP-induced CRH promoter activation was examined by using a luminometer and luciferase assay. Calorimetric Beta-galactosidase assays were performed to correct for transfection efficiency. Luciferase expression vectors of cAMP-downstream molecules, CRE and AP-1, were used to further examine the signaling cascades. Results: cAMP stimulation induced AP
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